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It's neat to see others with glucose metabolism issues benefiting from your encouragement to give CE a try. But I've been a bit underwhelmed by the Longecity community's response to the thread on CE you started. Really only you, me and Drew seem to have engaged on the thread...

--Dean

Agreed. I'm disappointed by LongeCity, but had low expectations going in. I'm still on the fence about whether I should update that thread or not? Part of me likes the idea of maintaining some sort of "summary" type thread that isn't 500 pages long like this one. Part of me also likes the idea of a "CE for dummies" type thread that I can send to people where they won't necessarily be overwhelmed (I'm not sure I can pull both off in a single thread though), even if there is little or no participation.

One downside to LongeCity is that they only allow edits for a few hours after you post. I like how our version here allows edits for far longer (forever?). This would allow me for example to just stick all the "sciency" summary type updates in the first post only, and anyone not interested could easily skip that. I also like the idea of being able to fix mistakes after the fact any time they are noticed.

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Neat glove-based cooling technology from Stanford. Not easy to reproduce though, with the vacuum it uses and all...

Yea, apparently the Stamford ones originally cost $1800, but they have a slicker commercial product now for $895. It won't be long until the cheap Chinese knockoffs hit the market and you'll be able to get one for $30. I have thought about creating my own, it would be challenging but not impossible. Vacuum could come from a vacuum cleaner, you'd need some copper tubing (home depot) and a pump (fish tank supplies) to circulate water which could be pulled maybe just from a 5 gallon bucket of water + ice. I'd love to give this a try. It looks like these are taking the sports world by storm, see:

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BAT and Cold Exposure Effects on Metabolic Rate and Glucose Metabolism in Healthy Men

I thought this new study [1] and several studies it references (e.g. [2][3]) were interesting because of how meticulously they documented the quantitative impact of being BAT-positive on various aspects of metabolism.

Each of these studies divided young healthy men into those who had detectable BAT (BAT+) vs. those who didn't (BAT-) based on PET imaging during cold exposure.

Study [2] focused on calorie expediture. Mild cold exposure (19°C = 66 °F) increased the average calorie expenditure of BAT+ men by +410 kcal/d, vs only +42 kcal/d in the BAT- men. The men with the most BAT showed the biggest increase in cold-induced calorie expenditure as can be seen in the following figures:

Study [1] found that among BAT+ men, diet-induced thermogenesis (the amount of heat produced after eating) was increased by about 60kcal/day on average - not all that much. The BAT+ men also burned more fat relative to carbohydrates (RQ of 0.86 vs. 0.89).

Of course these were random healthy young men, probably not intentionally subjecting themselves to cold exposure to build BAT. Interestingly, while these guys weren't rail-thin, on average the BAT+ men were slightly skinnier than their BAT- counterparts. In [1], the BMI of BAT+ vs. BAT- men were 20.0 vs. 21.4 and in [2], BAT+ vs. BAT- BMIs were 21.2 vs. 22.6.

So there is hope for us thin folks to develop BAT. I will note though that these guys were all in their 20s and the average age of BAT+ vs. BAT- men was 24 vs. 29, reinforcing the previous observation that BAT and BAT activity tends to go down with age.

Study [3] was interesting, because it validated what many of us have observed - namely that BAT improves insulin sensitivity and glucose metabolism. They found the BAT+ men had less visceral fat and more subcutaneous fat than the BAT- group, which is a good thing, since visceral fat is more associated with inflammation and metabolic syndrome. Cold exposure increased the resting energy expenditure of the BAT+ men by 15% relative to the BAT- men, which would be about 225 kcal/day.

But the really dramatic finding was in glucose disposal in response to cold exposure. Basically, they intravenously administered radioactive glucose to the men while they were in either thermoneutral vs. cold temperatures. As you can see from the graphs below, the BAT+ men showed large increases in their ability to clear glucose, as well as their insulin sensitivity during cold exposure:

This suggests to me that cold exposure soon after eating may dramatically reduce glucose excursions of folks with BAT.

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As anyone reading this will know by now, I'm a big fan Cool Fat Burner (CFB) cooling vest(s). But now that it's summertime and hot here in Pittsburgh, and I'm going through all my CFB cool packs (12 of them) during the course of the day. Additional cold packs from CFB are not cheap - $50 for a pack of four.

So I went looking online for alternatives, and boy did find a deal. Amazon sells these cold packs that are virtually identical to the "hardcore packs" sold by CFB. They are 6x10" and 24oz vs. the CFB packs which are 6x9" and 22oz. The extra 1" length is no problem, since the CFB pockets have plenty of extra room in that direction.

And you can't beat the price - they are $13 for a set of 9 ($1.46 ea), vs. $50 + $10 tax & shipping for a set of 4 from CFB ($15 ea). That is less than 1/10th the price! So that's part one of a really inexpensive DIY cooling vest...

Now the question is how to drape them to you body, without shelling out for the CFB vest, which cost $70 + shipping?

Ever the engineer, here is a free cooling vest solution I came up with, made from an old long-sleeve shirt and some safety pins. Here is a picture of the pinned shirt, to create four pockets for the ice packs, just like the "classic" CFB vest has:

You simply slip four frozen ice packs into the pockets through the shirt's neck hole, like this:

Then put it on over you head putting your head through the hole created by the pinned sleeves, in order to wear the shirt over you shoulders like a cape. Here is what it looks like on:

For anyone who wants to get fancy, you could sew along the lines of safety pins, and cut off the excess shirt material. But this way, I don't even ruin the shirt, in case the Steelers make it to the playoffs again this year (Go Steelers!). ☺

In short, with this DIY cooling vest and the Amazon ice packs (9x) above, you too can experiment with cold exposure for only $13. The equivalent from Cool Fat Burner would be $70 for the vest and four ice packs, plus another $50 for a second set of ice packs, or a total of $120. With tax and shipping the CFB equivalent comes to $141. So at $13, this DIY cooling vest solution is more than 90% off - Can't beat that!

Let me know what you think, and if anyone else tries it.

Happy chilling!

--Dean

P.S. For anyone wondering how I manage all those ice packs in my freezer, here is a rack I created for them out of some old corner freezer shelving to allow air circulation around the packs, and for easy transfer in/out of the freezer:

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Great homemade vest, and that IS a killer deal from Amazon (great reviews there) can't believe they sell them so inexpensively. They are in my cart... I still plan to make a vacuum cooler just to see if it lives up to the hype (it seems quite gimicky to me). I'll need to figure out some way of objectively measuring its relative performance.

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A swim or a cold shower would do the same thing right? Which brings up a ? I have had for some time.Dean, without pouncing on me please, I am wondering have you ever discussed the amount of time one needs to be exposed to cold to gain any benefits. I know you said it somewhere, but I really don't want to read all these posts to find it

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I am wondering have you ever discussed the amount of time one needs to be exposed to cold to gain any benefits. I know you said it somewhere, but I really don't want to read all these posts to find it

Sorry Mike. I realize now that the last time you asked this question I interpreted it too narrowly, to mean what temperature does it take to activate BAT in someone who already has it. My answer was "the low 60s °F".

What it takes to build BAT or beige adipose tissue is going to depend on a lot of things, including your heritage (Caucasian better than Asian or African), your genetics (best to be Being of genotype TT for rs1800592 and AA for rs4994 as reported by 23andMe), your gender (women better than men), your age (younger better than older) and your weight (not too fat or too thin - BMI in the low 20s appears best).

But here I discussed a study [1] with some concrete numbers for building BAT via cold exposure. If found exposure to 17 °C (62.5 °F) for2h/day for six weeks was enough to nearly triple the average cold-induced thermogenesis (~100 kcal/day → ~300 kcal/day) in healthy people who initially didn't have any BAT. Of the 8 initially BAT- men in the study, 6 of them (75%) showed detectable BAT activity by the end of six weeks of cold exposure.

Interestingly, this new study from last month [2], instructed some men to expose themselves to cold for six weeks in late winter in Sweden for at least one hour per day, while others (controls) were told to avoid cold whenever possible. After six weeks, the controls (left graph below) had nearly identical BAT volume to when they started. In contrast, after throwing out the two non-compliant men (highlighted in yellow below right), the men who exposed themselves to cold for six weeks (avg 79min / day) showed a modest increase in BAT volume, as measured by cold-induced BAT activity using PET imaging.

But the change in BAT activity was pretty modest. They saw a small decrease in metabolic rate of the warm controls (-50kcal/day), and a similar modest increase in metabolic rate of the cold-exposed group (+70kcal/day). This was true at both room temperature and in cold conditions.

The self-administered and self-reported nature of the cold-exposure in this study makes it less definitive. Nevertheless, it suggests that one hour per day of "casual" cold exposure may be enough to cause a modest increase in BAT volume and BAT activity. However this mild amount of cold exposure wasn't sufficient to result in changes in metabolic parameters of the subjects - i.e. none of the usual positive metabolic effects of cold exposure were observed (reduced weight, lower fasting insulin, lower fasting glucose). So one hour of casual cold exposure per day probably isn't enough to have much of a positive effect.

So "a couple hours per day of rigorous cold exposure for a few weeks" would be my answer to how much CE it probably takes to see positive results (e.g. improved glucose metabolism).

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Back in early July in a post flippantly titled Luigi Fontana - Missing the Obvious? I reviewed a new paper [1] by Luigi and colleagues about branch chain amino acid (BCAA) restriction, and especially Leucine restriction. What they found was summarized in the graphical abstract:

The authors weren't sure what the molecular pathway was that resulted in the metabolic benefits (reduced weight and improve insulin sensitivity without eating less or being more physically active):

[T]he ultimate molecular mechanism that drives the effect of a

leucine reduced diet on white adipose tissue is as yet unknown.

I speculated that it was likely an effect of the browning of white fat, based especially on another study on Leucine restriction (PMID 26643647 discussed here), that saw similar effects and traced it to increased UCP1 expression (i.e. browning) in white fat.

I sent an email to Luigi, inquiring if he'd considered this explanation, saying:

... Take a look at that post for more discussion of why it seems to me that BAT/beige fat thermogenesis is the likely explanation for your apparent mystery. I'd love to know what you think, and if I can post your response to the CR forums.

I thought he'd forgot or blew me off, but today he got back to me. Here is what he said:

Dear Dean,

Nice to hear from you.

Yes, we think that most likely this is the cause.

Animals were kept in metabolic cages and we found that physical activity was not increased and food consumption was not decreased. So, most likely there is BCAA induced uncoupling.

Yours,

Lu

So now we have it directly from luigi - Amino acid / BCAA / Leucine restriction probably improves metabolic healthy by turning white fat to brown.

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MR gets furious when he reads a post where someone claims "restriction" of any individual amino-acid. I don't think he'll like it if you make any claims about restricting BCAAs or leucine. How was such restriction achieved in humans according to PMID:27346343? According to the supplemental material:

On second thought, I hope Michael doesn't respond. Instead I'd really like him to read and analyze the new paper on the crazy metabolic impact of sucralose (and likely other artificial sweeteners) discussed here.

But you are right Tom, it would be interesting to know what modifications the folks in the WUSTL kitchen did to the diet of their human subjects to make it low in BCAAs and leucine.

--Dean

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Back in this post, I first pointed to evidence that resveratrol causes the browning of white fat (PMID: 25761413). This new study [1] published last month further confirms this association. They studied rat adipose tissue both in vitro and in vivo and found that:

Feeding mice resveratrol, either while eating standard chow or a high-fat diet, resulted in significant (p < 0.05) increases in the number of brown(ish) adipocytes and BAT weight.

Feeding mice resveratrol along with a high-fat diet more than doubled UPC1 expression (and AMPK expression) in fat cells, but the same boost in UCP1 expression from or resveratrol was not observed in rats fed normal chow.

Insulin sensitivity was improved with resveratrol feeding in both diet groups.

So this looks like confirmation that resveratrol boost brown fat and brown fat activity, particularly in the context of a diet with lots of fat.

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But here I discussed a study [1] with some concrete numbers for building BAT via cold exposure. If found exposure to 17 °C (62.5 °F) for 2h/day for six weeks was enough to nearly triple the average cold-induced thermogenesis (~100 kcal/day → ~300 kcal/day) in healthy people who initially didn't have any BAT. Of the 8 initially BAT- men in the study, 6 of them (75%) showed detectable BAT activity by the end of six weeks of cold exposure.

Thanks Dean. That is the kind of practical information I was looking for. I am so pleased because that sounds like a cinch. 2 hours a day at 60ish degrees.

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Michael has been understandably skeptical of the model of CR / CE synergy I proposed here and discussed further here. This model can be summarized in the rather complicated diagram below. Notice the yellow highlights? These represent aspects of the model that are supported by three papers [1][2][3] published in the last month:

Study [1] address the significance of SIRT1 for BAT activity. It found that mice genetically deficient in SIRT1 (SIRT1(+ /-)) expressed less SIRT1 in BAT tissue, and this deficit was accompanied by a decrease in mitochondrial DNA expression, reduced expression of UPC1, as well as a decrease in whole body oxygen consumption and an inability for the mice to keep warm during a cold challenge. In short, [1] suggests that SIRT1 is critical for maintaining proper function of BAT, by boosting mitochondria and UPC1 expression.

Study [2] looked at the importance of Protein Kinase A (PKA) for promoting BAT activity. Mice genetically programmed to overexpress PKA in adipose tissue were protected from getting obese on a high fat diet, and exhibited increased insulin sensitivity, glucose tolerance and pancreatic β-cell function - a topic many of us are concerned about as a result of the tendency of serious CR to impair glucose tolerance. They also expended more energy without eating more or being more physically active. The mechanism? - you guessed it, increased expression of UCP1 in subcutaneous WAT and BAT, and therefore increased thermogenesis.

In support of the above model, the authors conclude:

These data show that PKA activation is sufficient to induce

changes to a brown-like phenotype in the subcutaneous

WAT and to increase UCP1 expression in BAT.

The authors aren't sure how PKA increases the browning of WAT or increases BAT activity, saying:

Overall, although these studies alter adipose PKA

activity, they do not establish the functional effects of PKA

activity. The importance of our data is that it shows that

activation of PKA alone in adipose tissue is sufficient to induce

resistance to diet-induced obesity.

but there is good evidence that PKA is a mTOR regulator, and that mTOR is critical in the BAT synthesis and the browning of white fat, as we discussed here based on [4], which linked increased epinephrine (which is upregulated by cold) to elevated PKA activity in adipose tissue, which acted through mTOR1 (specifically the RAPTOR complex) to brown adipose tissue, independent of the insulin/AKT signalling pathway, exactly as shown in the diagram above.

Study [3] lends further support to the important role mTOR plays in WAT and BAT synthesis, and in insulin sensitivity. Mice that lacked mTOR in adipose tissue had decreased BAT and WAT mass, and were insulin resistant. They conclude:

Our study reveals the critical role of the mTOR signalling pathway in regulating

CR reduces insulin and IGF-1 signalling, which may have several good effects wrt inflammation and aging. But it also knocks down the anabolic action of mTOR, which can result in metabolic dysfunction (and impaired glucose tolerance in some of us), and reduced bone and muscle mass. These papers support the idea that cold exposure can overcome these negative effects of CR by activity mTOR via a separate pathway from insulin/IGF-1, involving PKA.

--Dean

------------

[1] Zhonghua Yi Xue Za Zhi. 2016 Jun 21;96(23):1859-62. doi:

10.3760/cma.j.issn.0376-2491.2016.23.017.

[Effect of SIRT1 deficiency on function of brown adipose tissue in obese mice].

[Article in Chinese]

Zheng XB(1), Ai HY, Yuan SH, Cao HY, Liang H, Weng JP, Xu F.

Author information:

(1)Department of Endocrinology and Metabolism, Third Affiliated Hospital, Sun

The in vivo role of mechanistic target of rapamycin (mTOR) in the development and function of adipose tissue, especially brown adipose tissue (BAT), is not well understood. Here, we aimed to assess the effect of mTOR (also known as Mtor) knockout on adipose tissues and systemic energy metabolism.

METHODS:

We generated adipocyte-specific mTOR-knockout mice (Adipoq-mTOR) by crossing adiponectin-Cre (Adipoq-Cre) mice with mTOR flox/flox mice. The mice were then subjected to morphological, physiological (indirect calorimetry, glucose and insulin tolerance tests) and gene expression analyses to determine the role of mTOR in adipose tissues.

RESULTS:

We provide in vivo evidence that mTOR is essential for adipose tissue development and growth. Deletion of mTOR decreased the mass of both BAT and white adipose tissues (WAT) and induced browning of WAT. In addition, ablation of mTOR in adipose tissues caused insulin resistance and fatty liver in the Adipoq-mTOR mice. Furthermore, mTOR was required for adipocyte differentiation in vivo and activation of PPARγ ameliorated the differentiation deficiency of the mTOR-null adipocytes.

CONCLUSIONS/INTERPRETATION:

Our findings demonstrate that mTOR is a critical regulator of adipogenesis and systemic energy metabolism. Our study provides key insights into the role of mTOR in adipose tissues; such knowledge may facilitate the development of novel strategies with which to treat obesity and related metabolic diseases.

During social interactions, our own physiological responses influence those of others. Synchronization of physiological (and behavioural) responses can facilitate emotional understanding and group coherence through inter-subjectivity. Here we investigate if observing cues indicating a change in another's body temperature results in a corresponding temperature change in the observer.

Methods

Thirty-six healthy participants (age; 22.9±3.1 yrs) each observed, then rated, eight purpose-made videos (3 min duration) that depicted actors with either their right or left hand in visibly warm (warm videos) or cold water (cold videos). Four control videos with the actors' hand in front of the water were also shown. Temperature of participant observers' right and left hands was concurrently measured using a thermistor within a Wheatstone bridge with a theoretical temperature sensitivity of <0.0001°C. Temperature data were analysed in a repeated measures ANOVA (temperature × actor's hand × observer's hand).

Results

Participants rated the videos showing hands immersed in cold water as being significantly cooler than hands immersed in warm water, F(1,34) = 256.67, p<0.001. Participants' own hands also showed a significant temperature-dependent effect: hands were significantly colder when observing cold vs. warm videos F(1,34) = 13.83, p = 0.001 with post-hoc t-test demonstrating a significant reduction in participants' own left (t(35) = −3.54, p = 0.001) and right (t(35) = −2.33, p = 0.026) hand temperature during observation of cold videos but no change to warm videos (p>0.1). There was however no evidence of left-right mirroring of these temperature effects p>0.1). Sensitivity to temperature contagion was also predicted by inter-individual differences in self-report empathy.

Conclusions

We illustrate physiological contagion of temperature in healthy individuals, suggesting that empathetic understanding for primary low-level physiological challenges (as well as more complex emotions) are grounded in somatic simulation.

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That temperature contagion paper is interesting. I looked into the details of the full text, and it appears that on average subjects watching a video of someone plunging one hand into an ice bath triggered about a 0.2 °C (0.36 °F) decrease in the skin temperature of the corresponding hand. The more empathetic your personality, the larger the change in skin temperature. Not a huge effect, but as you say, quite interesting. Vicarious cold exposure!

--Dean

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We've recently been discussing insulin resistance and glucose intolerance a lot (here and here), and how exercise and cold exposure can alleviate the problem of impaired glucose tolerance that some folks on severe CR have experienced.

One hypothesis for how glucose metabolism might be impaired in CR folks is that lack of muscle mass and lack of (brown) adipose tissue in severely CRed folks could leave no place for the glucose to go after a meal, so it remains in circulation, doing damage. Another hypothesis for glucose intolerance in general (not just in CR folks) is the so called "intramyocellular lipid" hypothesis, promoted most vocally by Dr. Neal Barnard, in fact just last week in this short video (warning: Facebook link).

But after looking into it a while back, I became somewhat skeptical of Dr. Barnard's explanation, at least in it's simplest form - that is, lipids inside muscle cells "gum up" the pathway by which glucose is transported from the blood into muscle cells to be burned as fuel. This review in particular [2] does a good job pointing out that the connection between intramyocellular lipids and insulin resistance is a lot more complicated than originally thought, and pointing out that lipid drops inside muscle cells serve important metabolic functions, foreshadowing this new paper [1] I'm highlighting today.

But before we get to [1], it's important to point out one apparent weakness of the "muscle lipid → insulin resistance" hypothesis. That is the fact that endurance athletes, who have very good insulin sensitivity, nevertheless have been shown to have elevated amounts of lipid droplets in their muscle cells, nearly as much as obese folks and diabetics in fact, a phenomenon referred to as the athlete’s paradox [3]. The authors of [3] summarized their findings (in 2001) as such:

In summary, skeletal muscle of trained endurance athletes is markedly insulin sensitive andhas a high oxidative capacity, despite having an elevated lipid content. Inconclusion, the capacity for lipid oxidation may be an important mediator of theassociation between excess muscle lipid accumulation and insulin resistance.

With that foreshadowing, I bet you can guess what today's paper [1] found. Yup, exercise turns the fat inside muscles to brown, making it metabolically active and able to burn more, rather than less, glucose.

In the paper, they used female C57BL/6 mice and (presumably) housed them at standard, chilly-for-mice lab temperature. They fed them either a standard or high-fat diet ad lib, and gave half of each group a running wheel for six hours per night. They ran two experiments with a group of mice that got the running wheel from the start for six weeks, or were fed the HFD for 12 weeks before being given the running wheel for an additional six weeks. The mice with the running wheel worked their little butts off as mice are prone to do when given a wheel, running an average of about 6 miles (10 km) per night! Given their size, that's a heck of a lot of endurance exercise!

In the high fat group, running prevented most of the diet-induced weight & fat mass gain. Interestingly, running did not increase muscle mass in the high fat exercise group relative to the high fat sedentary controls. Not surprisingly, the high fat diet increased lipids inside muscles in both the exercise and sedentary groups relative to the mice fed a standard, low-fat chow. Here is the all-important data showing lipid (triglyceride) content in muscle cells of the control (low-fat) diet mice (CTL), control diet + exercise mice (CTL-E), high fat diet mice (HFD), and high fat diet + exercise mice (HFD-E):

As you can see, in both sets of experiments, the muscles of the exercise mice showed a trend towards more fat in their muscles than the sedentary mice - recapitulating the athlete's paradox in mice. The difference was especially dramatic in the high fat diet mice (HFD vs. HFD-E).

Unfortunately, they didn't measure insulin sensitivity, but it's virtually certain that the exercise mice were more insulin sensitive than the sedentary controls, based on previous data in humans and mice of the effects of exercise on insulin sensitivity.

What they did measure were the mRNA level of proteins that are markers for brown adipose tissue inside the muscle cells of the various groups. Sure enough, UCP1 and the mitochondria-biogenesis-promoting PGC1α were dramatically elevated in the mice that exercised. In fact, UCP1 mRNA was increased by a factor of 100 - 200 in the experiment where access to the running wheel was delayed until the mice got pretty chubby (right graph below):

In short, the fat in the muscles of exercising mice was a lot "browner", meaning it augmented rather than impaired the ability of muscles to burn glucose, and hence serves to explain the athlete's paradox. Most interesting of all to me was this statement the concluding paragraph of the paper (my emphasis):

Additionally, HFD was additive to exercise in browning muscle lipid and, thus, exogenous lipid consumption may be a critical factor in the phenotypic shifts that occur with endurance training. This mouse model suggests that increased muscle lipid may represent a potential beige fat depot that serves the metabolic needs of exercise.

In other words, in order to benefit from insulin-sensitizing effects of endurance exercise, it looks like you may need to eat extra calories, and especially extra fat, in order to build up calorie-burning beige fat deposits in muscles.

It is no wonder therefore that rail-thin CR folks with very little skeletal muscle (and virtually no fat or brown fat), exhibit impaired glucose tolerance. Just as I've speculated elsewhere (here too), this study seems to confirm that they likely have too little muscle and fat to serve as sinks for the circulating glucose.

This also goes a long way towards explaining why exercise improves insulin sensitivity in obese and diabetic people, even without calorie restriction and without/before weight loss [4][5][6]. In a backhanded sort of way quite the opposite of what he intended, Michael is right. Health and longevity is not about the weight. But it's also not about the absolute number of calories either.

Gordo, still think the combination of cold exposure and endurance exercise is a counterproductive waste of time and energy?

Finally, these results make Michael's quip a while back about jiggling pecs as the explanation for thermogenesis and as a way to dismiss the benefits of cold exposure and exercise look even sillier... To quote my least favorite politician - "so sad."

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So Dean how would you sum it up for us dummies. My take is lots of intense exercise/running etc., resistance training several days a week, cold exposure 2 or more hours a day and say 40% fat. And yes I know Here I go again contradicting myself because I recently posted I was not going to micromanage, but your posts are irresistibly fascinating!!!

Also I thought you had decided intense/endurance exercise was not a good thing in anything like what these mice were doing?

"Do I contradict myself? Very well, then I contradict myself, I am large, I contain multitudes"

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Gordo, still think the combination of cold exposure and endurance exercise is a counterproductive waste of time and energy?

Yes, I do :)

I still love that we have quite different approaches and hope it stays that way, it will be interesting to see as more (if more?) people get involved, which approach the data ends up favoring (or perhaps there is no favorite). We both get 30-40% of calories from mostly unsaturated, plant based fat, so at least we agree on that, we also agree on the fact that muscles are a great tool for glucose control and are integral to optimal CE results.

I'm all about finding the most efficient ways of doing things. I never said no good could come from endurance exercise, but so far nothing that you have posted has convinced me that routine endurance exercise is the most efficient (optimal) way of reaching any of our health and longevity goals. One must also consider the downsides of serious regular endurance exercise - wearing out your joints and depleting your body of important resources. As you've pointed out, muscle mass is important for health and longevity (maximizing the benefits of CE), this is something I've been pounding the table on for a while. Is it more efficient to build muscle mass via 9 hours of stationary biking, 2 hours of jogging, or 10 minutes of intense anaerobic exercise like sprints, weight vest stair runs, pull ups, and hanging crunches? Excessive endurance exercise can in fact actually lead to net muscle loss. Comparing photos of different types of athletes should tell you which style results in muscle gains -- that said there aren't a whole lot of muscle bound athletes that eat a low protein plant based whole food diet and just being muscular in and of itself is NOT the goal and in fact many of the things people do to become muscular are counterproductive to health and longevity (particularly when it comes to diet and supplements).

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He'll come back to an empty pantry and a devastated "CR garden". But he must give us a full report on what he ate on vacation - cause that's always a problem for me... mostly, I just go off diet altogether when vacationing abroad - I start of trying to keep it together, but by the end of the first week, I usually delve into the local cuisine, especially if I'm somewhere exotic or simply renowned for great food (South of France, anybody...) :)

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On my recent 2 week road trip I tried to keep the diet, but ended up having "special exceptions". I did bring a cooler full of my usual foods though. We stopped at several supermarkets and loaded up on produce during the trip. There are actually a LOT of chain type places to buy good plant based whole food meals. Panera has a pretty nice cobb avocado salad that you can customize out the wazoo substituting the meat parts that normally come with it for all sorts of plant based goodness (best to do this using their app and just put your order in via the app). Chipotle, despite all the recent critics, is a great stop too -- I get their "bowl" full of black AND pinto beans (just ask for both and they will do it), brown rice, guac, tomatoes, peppers, onions, corn, lettuce. The Cheesecake Factory has a phenomenal "Super Antioxidant Salad" (yes, they actually call it that).

Anyway, so as not to stray off topic too much...

First - the cheap cooling towels arrived yesterday from China (I was surprised they arrived so quickly). They are GREAT, I highly recommend these things, I had one draped over me last night while under a ceiling fan and the evaporative cooling was quite strong. I need to look for a shirt made out of the same material.

In other news, we had recently discussed the most efficient ways of building muscle mass (for longevity promoting health benefits in particular with respect to cold exposure). My approach is HITT style bodyweight exercises, the following video is an example of this, and the guy in the video, Frank Medrano, is a vegan by the way:

These guys inspired me to install a pull up bar in my bedroom, it was a fun project, it hangs down from the ceiling and is mounted up in the attic, I just used simple, inexpensive galvanized pipe and pipe connectors from Home Depot. Since its right next to the bed, I have no excuses not to use it, and I do use it, pretty much every single day. My family also started using it:

Even my 4 year old daughter can do pull ups with a little assist (found that stretch band thing on Amazon):

(she even has great form)

-Gordo

Edited August 5, 2016 by Gordo

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Last week in this post I pointed to these ice packs on Amazon as alternatives to the ones sold with the Cool Fat Burner for 1/10th the price. They arrived and I had a chance to test them out today. They are indeed slightly longer and slightly heavier than the CFB ice packs. But they fit nicely in the pockets of both models of the CFB, and they seem to hold their temperature for approximately as long as the solid packs from CFB. So I highly recommend them for people looking for less expensive alternatives to the ice packs offered by CFB.

On a related note. I've discontinued my recent practice of wearing the CFB without a shirt, since I just noticed a bit of numbness to the touch in my shoulders, which has persisted for at several hours after removing the CFB. Don't want to overdo it... ☺

--Dean

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Here is yet another BAT Rule1example - this time it's dietary fiber. This new study [1] found that both oat and wheat fiber boost BAT and the browning of WAT, and helps to prevent obesity induced by a high fat diet.

In the study, researchers used seven-week-old male C57BL/6J mice housed at normal lab temperatures (22 °C). For 24 weeks they fed them either normal chow (Chow), a high fat diet (HFD), HFD + Oat fiber (H-oat) or HFD + Wheat fiber (H-wheat). The fibers accounted for 0.8% of diet by weight, and was mixed into their food.

The two HFD fiber groups gained less weight than the HFD-only group, and slightly more than the Chow-fed group. Protein Kinase A (PKA) which you'll recall is central to the "alternative anabolic pathway" I outlined most recently here, was higher in BAT in the H-wheat group and especially higher in WAT in the H-oat group as illustrated by the yellow bars below:

Other signs of browning were that Oat fiber increased expression of UCP1 in WAT, and both fibers boosted longevity-promoting FGF-21 as well as mitochondria-biosynthesis-promoting PGC-1α in both BAT and WAT. The activity of the β3 adrenergic receptor, which detects elevated norepinephrine that results from, among other things, cold exposure, was also increased by the fiber diets.

It's funny. I just recently ran out of the oat fiber samples I'd gotten for free of from Creafill, and instead ordered this oat fiber from Amazon. Ironically, I just received it today, the same day I discovered this study showing oat fiber helps brown WAT and boost BAT.

The oat fiber from Amazon It is a really nice fine powder, which I'll be using as part of my fiber mix (which also includes psyllium, potato starch & plantain flour) to thicken my blended fruit & veggie "salad dressing" - which Saul foolishly criticizes.

1BAT Rule - Virtually every dietary or lifestyle intervention that is known to be healthy is also associated with an increase in BAT activity, browning of white fat and/or thermogenesis.

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Here is the latest full list of modifiable and [nonmodifiable] factors associated with increased brown/beige adipose tissue and/or thermogenesis, with the factors mentioned in this post highlighted in red:

Dietary fiber consumption is associated with reduced risk for the development of noncommunicable diseases. The aim of the present study was to evaluate the effects of cereal dietary fiber on the levels of proteins involved in lipolysis and thermogenesis in white adipose tissue (WAT) and brown adipose tissue (BAT) of C57 BL/6 J mice fed a high-fat diet (HFD).

At the end of the feeding period, body and adipose tissues weight in both H-oat and H-wheat groups were lower than in the HFD group. Mice in the H-oat and H-wheat groups showed an increasing trend in serum adiponectin level. Compared with the HFD group, cereal dietary fiber increased protein expressions involved in the lipolysis and browning process. Compared with the H-wheat group, H-oat was more effective in protein expressions of PKA, PGC-1 α, and UCP1 of the WAT samples. Compared with the H-oat group, H-wheat was more effective in protein expressions of PKA, ATGL, UCP1, β3AR, and FGF-21 of the BAT samples.